Summary In a variety of adult and childhood leukaemia cell samples collected at different states of the disease, we analysed in a series of sequentially performed slot-blot or Northern-blot hybridisation experiments the expression of genes possibly involved in multiple drug resistance (MDR) (mdrl/P-glycoprotein, DNA topoisomerase II, glutathione-S-transferase x), and the expression of the DNA topoisomerase I and histone 3.1 genes. Occasionally, P-glycoprotein gene expression was additionally examined by indirect immunocytofluorescence using the monoclonal antibody C219. No significant difference in mdrl/P-glycoprotein mRNA levels between primary and relapsed state acute lymphocytic leukaemias (ALL) was seen on average. Second or third relapses, however, showed a distinct tendency to an elevated expression of this multidrug transporter gene (up to 10-fold) in part well beyond the value seen in the moderately cross-resistant T-lymphoblastoid CCRF-CEM subline CCRF VCR 100. Increased mdrl/P-glycoprotein mRNA levels were also found in relapsed state acute myelogeneous leukaemias (AML), and in chronic lymphocytic leukaemias (CLL) treated with chlorambucil and/or prednisone for several years. Topoisomerase I and topoisomerase II mRNA levels were found to be very variable. Whereas in all but one case of CLL topoisomerase II mRNA was not detected
Summary The distribution of Gp 170, a multidrug resistance (MDR) associated glycoprotein, also called P-glycoprotein (P-gp), was examined by immunohistochemistry, using C219 and MRK16 monoclonal antibodies. Sixty-five tumour tissues were studied which included 40 non-lymphoid tumours, 15 chemoresistant non-Hodgkin's lymphomas and 10 Hodgkin's disease. The study was performed on both cryostat and special fixation processed and paraplast embedded (ModAMeX) sections. The latter method preserves fixationsensitive antigens such as P-gp and allows a more precise morphological identification of neoplastic and non-neoplastic cell populations in contrast to cryostat sections. Immunohistochemical expression of P-gp was expected and confirmed in many non-lymphoid tumours, but stromal macrophages and endothelial cells were also frequently stained in these cases. In non-Hodgkin's lymphomas, cells that were stained with both C219 and MRK16 monoclonal antibodies on cryostat sections were identified as macrophages and endothelial cells and not neoplastic lymphoid cells, by the ModAMeX technique. These findings suggest that the quantitative assessment of MDR RNA by Northern blotting performed on fresh homogenates overestimates the MDR content of neoplastic cells in a number of lymphoid and non-lymphoid tumours. In addition, the mechanism of chemoresistance in non-Hodgkin's lymphomas is less likely to be associated with P-gp expression.
SUMMARYAmong 44 fully protected, late convalescent adults re-exposed to measles, four developed an asymptomatic secondary immune response (SIR) with a significant increase in measles virus (MV)-specific IgG and low IgM. The boosted antibodies were mainly of the IgG1 subclass and reacted with the nucleoprotein and the haemagglutinin protein. About 30 weeks after re-exposure, antibody levels had decreased by 35-50%, suggesting that the booster effect may only be transient. SIR was only found in individuals with a pre-exposure
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